The primary objective of this study was to determine the concentration-response relationship of the adenosine A1-receptor antagonist, BG9719 above, and in combination with furosemide on sodium excretion. The study population consists of adult subjects with symptomatic moderate to severe heart failure and renal insufficiency. BG9719 is a highly receptive adenosine A1-receptor antagonist that causes natiuresis by reducing adenosine A1-mediated sodium reabsorption in both the proximal and the distol tubules of the nephron with only minimal potassium loss. Maintenance of GFR is accomplished by BG9719's interruption of the tubuloglomerular feedback loop.